Evidence of oxidative stress in chronic heart failure in humans

J McMurray1, M Chopra, I Abdullah

  • 1Department of Cardiology, Western Infirmary, Glasgow, Scotland.

European Heart Journal
|November 1, 1993
PubMed

Insights

Oxidative stress (OS) is elevated in chronic heart failure (CHF), regardless of coronary artery disease (CAD). This study confirms OS markers are abnormal in CHF patients, indicating a need for further research into its causes and treatments.

Area of Science:

  • Cardiology
  • Biochemistry
  • Oxidative Stress Research

Background:

  • Chronic heart failure (CHF) is linked to increased oxidative stress (OS), indicated by elevated thiobarbituric reactive substances (TBARS) and reduced plasma thiol (PSH).
  • It remains unclear if OS is a consequence of coronary artery disease (CAD) or CHF itself.

Purpose of the Study:

  • To investigate whether OS is caused by CAD or CHF per se.
  • To identify a broader range of specific OS markers that are abnormal in CHF patients.

Main Methods:

  • Comparison of plasma TBARS and PSH levels in patients with CHF due to CAD versus non-CAD CHF against controls.
  • Analysis of additional OS markers, including malondialdehyde, erythrocyte superoxide dismutase, caeruloplasmin oxidase, erythrocyte glutathione, and plasma conjugated dienes in CHF patients and controls.

Main Results:

  • Both CAD-related CHF and non-CAD CHF groups exhibited significantly higher TBARS and lower PSH compared to controls.
  • CHF patients showed elevated malondialdehyde and reduced PSH.
  • Significant alterations in erythrocyte superoxide dismutase, caeruloplasmin oxidase, and erythrocyte glutathione were observed in CHF patients.

Conclusions:

  • Oxidative stress is a significant factor in chronic heart failure, independent of the underlying cause (CAD or non-CAD).
  • A comprehensive panel of OS markers is indeed abnormal in CHF patients, underscoring the systemic impact of oxidative damage.

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